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01.12.2012 | Research | Ausgabe 1/2012 Open Access

Journal of Inflammation 1/2012

Induction of intestinal pro-inflammatory immune responses by lipoteichoic acid

Zeitschrift:
Journal of Inflammation > Ausgabe 1/2012
Autoren:
Mojgan Zadeh, Mohammad W Khan, Yong Jun Goh, Kurt Selle, Jennifer L Owen, Todd Klaenhammer, Mansour Mohamadzadeh
Wichtige Hinweise

Electronic supplementary material

The online version of this article (doi:10.​1186/​1476-9255-9-7) contains supplementary material, which is available to authorized users.

Competing interests

The authors declare that they have no competing interests.

Authors' contributions

MZ and MWK carried out all animal work, immunocytochemistry (i.e., high throughput and confocal imaging) and flow cytometry experiments. Additionally, MZ and MWK gathered the raw data and using statistical analyses and graphic programs compiled the data into meaningful information. MZ, MWK, JLO also contributed to writing the Methods section of the manuscript. MZ and MWK collected all of the graphics and formed the figures of the Manuscript. YJG, TK designed experiments and contributed to writing the Methods section. KS performed Slp proteome analysis on NCK2031 strain. MM designed experiments, discussed and wrote the manuscript. All authors have read and approved this manuscript.

Abstract

Background

The cellular and molecular mechanisms of inflammatory bowel disease are not fully understood; however, data indicate that uncontrolled chronic inflammation induced by bacterial gene products, including lipoteichoic acid (LTA), may trigger colonic inflammation resulting in disease pathogenesis. LTA is a constituent glycolipid of Gram-positive bacteria that shares many inflammatory properties with lipopolysaccharide and plays a critical role in the pathogenesis of severe inflammatory responses via Toll-like receptor 2. Accordingly, we elucidate the role of LTA in immune stimulation and induced colitis in vivo.

Methods

To better understand the molecular mechanisms utilized by the intestinal microbiota and their gene products to induce or subvert inflammation, specifically the effect(s) of altered surface layer protein expression on the LTA-mediated pro-inflammatory response, the Lactobacillus acidophilus s urface l ayer p rotein (Slp) genes encoding SlpB and SlpX were deleted resulting in a SlpB- and SlpX- mutant that continued to express SlpA (assigned as NCK2031).

Results

Our data show profound activation of dendritic cells by NCK2031, wild-type L. acidophilus (NCK56), and purified Staphylococcus aureus-LTA. In contrary to the LTA-deficient strain NCK2025, the LTA-expressing strains NCK2031 and NCK56, as well as S. aureus-LTA, induce pro-inflammatory innate and T cell immune responses in vivo. Additionally, neither NCK2031 nor S. aureus-LTA supplemented in drinking water protected mice from DSS-colitis, but instead, induced significant intestinal inflammation resulting in severe colitis and tissue destruction.

Conclusions

These findings suggest that directed alteration of two of the L. acidophilus NCFM-Slps did not ameliorate LTA-induced pro-inflammatory signals and subsequent colitis.
Zusatzmaterial
Authors’ original file for figure 1
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Authors’ original file for figure 6
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Literatur
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